银屑病
免疫学
发病机制
趋化因子
生物
炎症
细胞因子
免疫系统
先天免疫系统
肿瘤坏死因子α
T细胞
树突状细胞
作者
Francesca Chamian,James G. Krueger
标识
DOI:10.1097/01.bor.0000129715.35024.50
摘要
An interactive network of inflammatory cytokines, chemokines, dendritic cells, and type 1 T cells or natural killer T cells potentially drives pathogenic inflammation in psoriasis vulgaris. Continued clinical studies with defined immune antagonists provide a critical means to dissect the contribution of different cell subsets and genomic pathways to the pathogenesis of psoriasis vulgaris.
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